“ beta blocker therapy has been shown to...

“... beta blocker therapy has been shown to cause...

weight gain... and to significantly increase

the risk of developing diabetes.”— Franz Messerli, MD,

European Heart Journal, 2003© Copyright 2009 - Larry Hobbs @ FatNews.com, All Rights Reserved

Thursday, June 18, 2009

http://www.FatNews.com


Beta blockers include drug like atenolol (Tenormin) and propranolol (Inderal).

© Copyright 2009 - Larry Hobbs @ FatNews.com, All Rights Reserved




Hi, this is Larry Hobbs @ FatNews.com





European Heart Journal, March 2003, 24(6): 487-9© 2009, Larry Hobbs, FatNews.com

Hotline Editorial

The LIFE study: the straw that should break thecamel's back

Franz H. Messerli*

Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121, USA

In the LIFE study, the most recent landmark trialin hypertension,1–3 more than 9000 hypertensivepatients were randomized to either a losartan-

reliable and more powerful surrogate endpoint forcardiovascular fatal and non-fatal events thanblood pressure per se.9,10 What has not clearly been

European Heart Journal (2003) 24, 487–489





allow us to explain the discrepancy betweencerebral and cardiac events in the losartan arm.12

2. We should not forget that there were small,albeit distinct, differences between the two treat-ment arms. Although blood pressure seemed tohave been reduced to a very similar level, closescrutiny of the blood pressure curves in the diabeticpopulation2 shows that systolic pressure was con-sistently higher and diastolic pressure consistentlylower in patients on atenolol compared with thoseon losartan. This is not surprising since beta-blockers have a negative chronotropic effect andincrease stroke volume to some extent, which inturn usually leads to an increase (or to a lesser fall)in pulse pressure than is seen with vasodilatoryagents such as losartan which do not affect strokevolume. In the betablocker compared with thelosartin group, more patients withdrew fromdouble-blind medication (27.1 vs. 22.6%; P<0.001),whereas fewer proceeded to combination therapy

lic hypertension.3 However, the statement in thismanuscript, “Previous intervention studies in ISHwith diuretics or beta-blockers or calcium antago-nists or angiotension converting enzyme inhibitorshave shown 36%, 42% and 38% reductions in strokeor placebo. A further 40% reduction in stroke withlosartan-based therapy is an important finding”, isdisturbing. The authors seemingly want us tobelieve that had losartan been compared toplacebo, a reduction in stroke in the order of mag-nitude of 80% would have been achieved. The ref-erences that they give for their statements areSyst-Eur, Syst-China, and SHEP. None of thesestudies documented a stroke reduction with beta-blockers (or ACE inhibitors). Given that in patientswith isolated systolic hypertension there was arobust 40% difference in stroke reduction betweenlosartan and atenolol, there seems to be littleneed to inflate these findings by a deceptivestatement.

488 Hotline Editorial




observed in the study could be explained, at least

3. Last, but not least, we should also scrutinizethe efficacy of the comparator to losartan, i.e.

beta-blockers were no better than placebo, and when-

14

the risk of cardiovascular morbidity and mortalityparadoxically increased. Even in the younger hyper-

beta-blockers only have beenshown to reduce events in male non-smokers. Therisk of strokes was between two and four times

14

benefits that were similar to captopril, there wasno significant reduction in coronary artery disease,sudden death or MI. On the contrary, beta-blockertherapy has been shown to cause systematic weightgain19 and to significantly increase the risk ofdeveloping diabetes.20 Given the known spottyrecord of beta-blockers in the diabetic population,the superiority of an angiotensin receptor inhibitorin the LIFE study in these patients is hardly asurprise.

Thus, to put it somewhat pointedly, a losartan-based regimen did not reduce MI more than placebo(i.e. atenolol), but showed efficacy in reducing


“... On the contrary, beta blocker therapy has been shown to cause... weight gain...”

— Franz Messerli, MD




observed in the study could be explained, at least

3. Last, but not least, we should also scrutinizethe efficacy of the comparator to losartan, i.e.

beta-blockers were no better than placebo, and when-

14

the risk of cardiovascular morbidity and mortalityparadoxically increased. Even in the younger hyper-

beta-blockers only have beenshown to reduce events in male non-smokers. Therisk of strokes was between two and four times

14

benefits that were similar to captopril, there wasno significant reduction in coronary artery disease,sudden death or MI. On the contrary, beta-blockertherapy has been shown to cause systematic weightgain19 and to significantly increase the risk ofdeveloping diabetes.20 Given the known spottyrecord of beta-blockers in the diabetic population,the superiority of an angiotensin receptor inhibitorin the LIFE study in these patients is hardly asurprise.

Thus, to put it somewhat pointedly, a losartan-based regimen did not reduce MI more than placebo(i.e. atenolol), but showed efficacy in reducing


“... and to significantly increase the risk of developing diabetes.”





to withdraw from beta-blocker therapy. This ishardly an acceptable risk/benefit ratio for a com-pletely asymptomatic disorder such as hyperten-sion, and it is not surprising that losartan was muchbetter tolerated than atenolol in the LIFE study. Ina meta-analysis of all trials in a total of 16,164patients over age 60 whose average age was similaras in the LIFE study, beta-blockers did not reducefatal or non-fatal MIs, cardiovascular and all cause

For practicalpurposes, the comparator of losartan in the LIFEstudy, i.e. atenolol, must therefore be considereda placebo. Not surprisingly, the superiority of

only in about 10% of all patients with monotherapy,the lesser of the two evils. Underscoring thesuperiority of losartan over atenolol, Brunner andGavras21 wrote an accompanying editorial with thetitle, “Angiotensin blockade in hypertension: apromise fulfilled”. Mutatis mutandis one couldchange the title of this editorial to “Beta-blockersin hypertension—a promise broken”. This semanticissue notwithstanding, the LIFE study should beconsidered as the final straw that will break thecamel's back and hopefully motivate physiciansto no longer expose their elderly hypertensivepatients to the cost, inconvenience, adverse


“... one could change the title of this editorial to‘Beta-blockers in hypertension—

a promise broken.’”— Franz Messerli, MD




a meta-analysis of all trials in a total of 16,164patients over age 60 whose average age was similaras in the LIFE study, beta-blockers did not reducefatal or non-fatal MIs, cardiovascular and all cause

For practicalpurposes, the comparator of losartan in the LIFEstudy, i.e. atenolol, must therefore be considereda placebo. Not surprisingly, the superiority oflosartan over atenolol was even more pronouncedin the subgroup of 1326 patients with isolated systo-

promise fulfilled”. Mutatis mutandis one couldchange the title of this editorial to “Beta-blockersin hypertension—a promise broken”. This semanticissue notwithstanding, the LIFE study should beconsidered as the final straw that will break thecamel's back and hopefully motivate physiciansto no longer expose their elderly hypertensivepatients to the cost, inconvenience, adverseeffects, and most importantly, to the inefficacy ofbeta-blockers.





patients over age 60 whose average age was similaras in the LIFE study, beta-blockers did not reducefatal or non-fatal MIs, cardiovascular and all cause

For practicalpurposes, the comparator of losartan in the LIFEstudy, i.e. atenolol, must therefore be considereda placebo. Not surprisingly, the superiority oflosartan over atenolol was even more pronouncedin the subgroup of 1326 patients with isolated systo-

change the title of this editorial to “Beta-blockersin hypertension—a promise broken”. This semanticissue notwithstanding, the LIFE study should beconsidered as the final straw that will break thecamel's back and hopefully motivate physiciansto no longer expose their elderly hypertensivepatients to the cost, inconvenience, adverseeffects, and most importantly, to the inefficacy ofbeta-blockers.


“... [this study will] hopefully motivate physicians to no longer expose their elderly hypertensive patients... to the inefficacy of beta blockers.”





Hotline Editorial

The LIFE study: the straw that should break thecamel's back

Franz H. Messerli*

Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121, USA

In the LIFE study, the most recent landmark trialin hypertension,1–3 more than 9000 hypertensivepatients were randomized to either a losartan-

reliable and more powerful surrogate endpoint forcardiovascular fatal and non-fatal events thanblood pressure per se.9,10 What has not clearly been

European Heart Journal (2003) 24, 487–489

Franz H. Messerli, MDOchsner Clinic, Section on Hypertension1514 Jefferson HwyNew Orleans, LA 70121(504) 842-4077 phone(504) 842-3144 phone(504) 842-4220 [email protected]



mailto:[email protected]

mailto:[email protected]



Do not be fooled into thinking that

just because a drug lowers blood pressure, ...





... or blood sugar...





... or cholesterol...





... that it must be good for you.





This is NOT necessarily so.





The only thing that matter is how the drug affects your Total Risk of Death.





I believe that potassium bicarbonate is vastly

superior to beta blockers...





and the other blood pressure medicines...





... for improving health.





I’ve been taking 1000 mg of potassium twice a day

(2000 mg per day) in the form of potassium bicarbonate since 2000.





My blood pressure dropped from roughly

140/80 mm Hg to124/73 mm Hg.





WARNING: Only take potassium under a

doctor’s supervision. Too much potassium

can kill you.





Eur J Nutr 40 : 200–213 (2001)© Steinkopff Verlag 2001

! Summary Theoretically, we hu-mans should be better adaptedphysiologically to the diet our an-cestors were exposed to during mil-lions of years of hominid evolutionthan to the diet we have been eatingsince the agricultural revolution amere 10,000 years ago, and since in-dustrialization only 200 years ago.Among the many health problemsresulting from this mismatch be-tween our genetically determinednutritional requirements and ourcurrent diet, some might be a con-sequence in part of the deficiency of potassium alkali salts (K-base),which are amply present in theplant foods that our ancestors ate in abundance, and the exchange ofthose salts for sodium chloride(NaCl), which has been incorpo-rated copiously into the contempo-rary diet, which at the same time ismeager in K-base-rich plant foods.

Deficiency of K-base in the dietincreases the net systemic acid loadimposed by the diet. We know thatclinically-recognized chronic meta-bolic acidosis has deleterious ef-

Received: 10 May 2001Accepted: 23 May 2001

Anthony Sebastian, M. D. (!)Box 0126University of CaliforniaSan Francisco, CA 94143, USATel.: +1-4 15/4 76-11 60Fax: +1-4 15/4 76-09 86E-Mail: [email protected]

fects on the body, including growthretardation in children, decreasedmuscle and bone mass in adults,and kidney stone formation, andthat correction of acidosis canameliorate those conditions. Is itpossible that a lifetime of eating di-ets that deliver evolutionarily su-perphysiologic loads of acid to thebody contribute to the decrease inbone and muscle mass, and growthhormone secretion, which occurnormally with age? That is, are con-temporary humans suffering fromthe consequences of chronic, diet-induced low-grade systemic meta-bolic acidosis?

Our group has shown that con-temporary net acid-producing di-ets do indeed characteristicallyproduce a low-grade systemicmetabolic acidosis in otherwisehealthy adult subjects, and that thedegree of acidosis increases withage, in relation to the normally oc-curring age-related decline in renalfunctional capacity. We also foundthat neutralization of the diet netacid load with dietary supplementsof potassium bicarbonate (KHCO3) improved calcium andphosphorus balances, reducedbone resorption rates, improvednitrogen balance, and mitigated thenormally occurring age-related de-cline in growth hormone secretion– all without restricting dietaryNaCl. Moreover, we found that co-administration of an alkalinizing

salt of potassium (potassium cit-rate) with NaCl prevented NaClfrom increasing urinary calciumexcretion and bone resorption, asoccurred with NaCl administrationalone.

Earlier studies estimated dietaryacid load from the amount of ani-mal protein in the diet, inasmuchas protein metabolism yields sulfu-ric acid as an end-product. Incross-cultural epidemiologic stud-ies, Abelow [1] found that hip frac-ture incidence in older women cor-related with animal protein intake,and they suggested a causal rela-tion to the acid load from protein.Those studies did not consider theeffect of potential sources of basein the diet. We considered that esti-mating the net acid load of the diet(i. e., acid minus base) would re-quire considering also the intake ofplant foods, many of which are richsources of K-base, or more pre-cisely base precursors, substanceslike organic anions that the bodymetabolizes to bicarbonate. In fol-lowing up the findings of Abelow etal., we found that plant food intaketended to be protective against hipfracture, and that hip fracture inci-dence among countries correlatedinversely with the ratio of plant-to-animal food intake. These findingswere confirmed in a more homoge-neous population of white elderlywomen residents of the U. S.

These findings support affirma-

ORIGINAL CONTRIBUTION

L. FrassettoR. C. Morris, Jr.D. E. SellmeyerK. ToddA. Sebastian

Diet, evolution and agingThe pathophysiologic effects of the post-agriculturalinversion of the potassium-to-sodium and base-to-chloride ratios in the human diet

They have found that potassium bicarbonate:• Reduce muscle loss• Reduces bone loss

• Increases growth hormone


Potassium chloride reduced blood pressure in older people from

160/89 to 145/81 mm Hg.


Potassium chloride reduced blood pressure in older people from

160/89 to 145/81 mm Hg.

1750-2300 mg of potassium per day lowered systolic pressure by 15 point and

diastolic pressure by 8 points.


Why not try potassium (bicarbonate) first?





Daniel Amen, MD, a psychiatrist and author of

“A Magnificent Mind at Any Age”,said on Public Television...





He uses natural treatments “whenever possible”.

— Daniel Amen, MD, psychiatrist





“I use medication in my practice, but it’s NOT

the first thing that I use.”






“I always think about the least toxic, most effective treatment.”






“And often, with [psyciatric conditions] [I treat them] with...”






“... natural supplements [first]...”






“So in my mind, I think, why not at least try that first?”






I have to ask the same question about blood pressure...





Why not try potassium (bicarbonate) first?





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